Mediators of Inflammation / 2018 / Article / Fig 10

Research Article

Epithelial Cells Attenuate Toll-Like Receptor-Mediated Inflammatory Responses in Monocyte-Derived Macrophage-Like Cells to Mycobacterium tuberculosis by Modulating the PI3K/Akt/mTOR Signaling Pathway

Figure 10

Scheme showing a possible mechanism of the alleviated TLR-mediated inflammatory responses of macrophage U937 cells to the mycobacterial infection by coinfected A549 epithelial cells. In a coinfected condition, the undefined signaling from H37Rv mycobacteria-infected epithelial cells could reduce TLR-mediated inflammation of macrophages via the PI3K/Akt/mTOR signaling axis, but not the PI3K/Akt/GSK3β pathway. Upon a coinfection of epithelial cells and macrophages to Mtb, the inflammatory responses in both host cell types were triggered in alveoli. In order to maintain the homeostasis of the alveolar microenvironment, the Mtb infection-induced epithelial cells subsequently alleviated the inflammation of the alveolar environment to secret soluble cytokines or mediators, which in turn inhibited the TLR-mediated inflammatory responses in macrophages to Mtb via the PI3K/Akt/mTOR pathway.

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